| 1. |
- Engström, Martin, et al.
(författare)
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An in vitro evaluation of standard rotational thromboelastography in monitoring of effects of recombinant factor VIIa on coagulopathy induced by hydroxy ethyl starch
- 2005
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Ingår i: BMC Blood Disorders. - : Springer Science and Business Media LLC. - 1471-2326. ; 5
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Rotational thromboelastography (ROTEG) has been proposed as a monitoring tool that can be used to monitor treatment of hemophilia with recombinant factor VIIa (rFVIIa). In these studies special non-standard reagents were used as activators of the coagulation. The aim of this study was to evaluate if standard ROTEG analysis could be used for monitoring of effects of recombinant factor VIIa (rFVIIa) on Hydroxy Ethyl Starch-induced dilutional coagulopathy. METHODS: The study was performed in vitro on healthy volunteers. Prothrombin time (PT) and ROTEG analysis were performed after dilution with 33% hydroxy ethyl starch and also after addition of rFVIIa to the diluted blood. RESULTS: PT was impaired with INR changing from 0.9 before dilution to 1.2 after dilution while addition of rFVIIa to diluted blood lead to an overcorrection of the PT to an International Normalized Ratio (INR) value of 0.6 (p = 0.01). ROTEG activated with the contact activator ellagic acid was impaired by hemodilution (p = 0.01) while addition of rFVIIa had no further effects. ROTEG activated with tissue factor (TF) was also impaired by hemodilution (p = 0.01) while addition of rFVIIa lead to further impairment of the coagulation (p = 0.01). CONCLUSIONS: The parameters affected in the ROTEG analysis were Clot Formation Time and Amplitude after 15 minutes while the Clotting Time was unaffected. We believe these effects to be due to methodological problems when using standard activators of the coagulation in the ROTEG analysis in combination with rFVIIa.
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| 2. |
- Jacobson, Annica, et al.
(författare)
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Can mutations in ELA2, neutrophil elastase expression or differential cell toxicity explain sulphasalazine-induced agranulocytosis?
- 2004
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Ingår i: BMC Blood Disorders. - : Springer Science and Business Media LLC. - 1471-2326. ; 4:1, s. 5-
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Drug-induced agranulocytosis, a severe side effect marked by a deficit or absolute lack of granulocytic white blood cells, is a rare side-effect of the anti-inflammatory drug sulphasalazine. Mutations in the human neutrophil elastase gene (ELA2), causing increased intracellular concentration of this serine protease, inhibits neutrophil differentiation in severe congenital neutropenia (SCN). Since the clinical symptoms of agranulocytosis and SCN are similar, we hypothesized that it may origin from a common genetic variation in ELA2 or that sulphasalazine may affect human neutrophil elastase activity and protein expression. METHODS: We screened for genetic differences in ELA2 in DNA from 36 patients who had suffered from sulphasalazine-induced agranulocytosis, and compared them with 72 patients treated with sulphasalazine without blood reactions. We also performed in vitro studies of the blood cell lines HL60 and U937 after sulphasalazine exposure with respect to cell survival index, neutrophil elastase protein expression and activity. RESULTS: None of the mutations in ELA2, which previously have been reported to be associated with SCN, was found in this material. Protein expression of human neutrophil elastase in lymphoma U937 cells was not affected by treatment with concentrations equivalent to therapeutic doses. Cell survival of lymphoma U937 and promyelocytic leukemia HL-60 cells was not affected in this concentration range, but exhibited a decreased proliferative capacity with higher sulphasalazine concentrations. Interestingly the promyelocytic cells were more sensitive to sulphasalazine than the lymphoma cell line. CONCLUSION: Neutrophil elastase expression and ELA2 mutations do, however, not seem to be involved in the etilogy of sulphasalazine-induced agranulocytosis. Why sulphasalazine is more toxic to promyelocytes than to lymphocytes remains to be explained.
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| 3. |
- Juto, Hans, et al.
(författare)
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Epidemiology of Adult Ankle Fractures : 1756 cases identified in Norrbotten County during 2009–2013 and classified according to AO/OTA
- 2018
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Ingår i: BMC Musculoskeletal Disorders. - : BMC. - 1471-2474. ; 19
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Tidskriftsartikel (refereegranskat)abstract
- Background: The ankle fracture is one of the most common fractures, increasing in an ageing population, but not generally seen as an osteoporotic fracture. The aim of this study was to examine the relationship between different AO/OTA classes of ankle fractures, age, sex and type of trauma.Methods: Ankle fractures, treated at any of the hospitals in Norrbotten County in Sweden between 2009 and 2013, were retrospectively identified and classified according to the AO/OTA-classification system. Information about the trauma mechanism was also obtained.Results: In Norrbotten County, 1756 ankle fractures in 1735 patients aged 20 years or older were identified. This gave an incidence in the county of 179 per 100,000 person-years. Of these patients, 34.6% were 65 years or older, 58.4% were women and 68.2% of the trauma leading to a fracture was defined as low-energy. In 1.5% of the cases the fractures were open. Incidences of type B fractures increased substantially with age, from 62 (95% CI 50–77) at 30–39 years of age to 158 (95% CI 131–190) in patients older than 80 years of age per 100,000 person-years. Type B fractures showed a slightly higher proportion of low-energy trauma while type C showed a lower mean age and proportion of women.Conclusions: This study shows an incidence of 179 adult ankle fractures annually per 100,000 persons. More than two thirds of the fractures were caused by a low-energy trauma and ankle fractures are more frequent among females. Females generally have an increased incidence during their life, mainly between the ages of 30 and 60. This is in contrast to men who have more of an even distribution throughout their life. Classification according to AO/OTA reveals some heterogeneity among the classes of ankle fractures in age and gender as well as the energy involved in the trauma.
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| 4. |
- Lilja-Lund, Otto, 1981-, et al.
(författare)
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Longitudinal neuropsychological trajectories in idiopathic normal pressure hydrocephalus : a population–based study
- 2023
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Ingår i: BMC Geriatrics. - : BioMed Central (BMC). - 1471-2318. ; 23:1
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Tidskriftsartikel (refereegranskat)abstract
- Background: Idiopathic normal pressure hydrocephalus (iNPH) is a progressive syndrome affecting gait, incontinence, and cognition in a significant number of older adults. Still, prospective studies on early development of symptoms are scarce.Aim: To investigate how neuropsychological functions develop before and in already diagnosed iNPH over a two-year period in a population-based material.Method: A sample of 104 participants (median [IQR] 75 [72–80] years old) from the general population underwent CT-imaging and clinical assessment at baseline and follow-up. We used the iNPH symptom scale covering four domains (Neuropsychology, Gait, Balance, Incontinence) and additional tests of executive functions. Morphological signs were rated with the iNPH Radscale. Non-parametric statistics with Bonferroni corrections and a significance-level of p < 0.05 were used.Results: Median (IQR) time to follow-up was 25 (23–26) months. Effect size (ES) for individuals who developed iNPH (n = 8) showed a large (ES r = -0.55) decline in the Gait domain and on the Radscale (ES r = -0.60), with a medium deterioration in declarative memory (ES r = -0.37). Those having iNPH at baseline (n = 12) performed worse on one executive sub-function i.e., shifting (p = 0.045).Conclusion: Besides deterioration in gait and radiology, our results suggest that a neuropsychological trajectory for those developing iNPH includes a reduction in declarative memory. Executive dysfunction was limited to those already having iNPH at baseline. These findings could suggest that memory impairments are included in the early development of iNPH.
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